1. ACNE Disorders of sebaceous gland
Omar Abdulaziz Al-Sheikh, M.D.
College of Medicine
King Saud University

2. Definition:
Is a chronic inflammatory disorder of the pilosebaceous apparatus of certain body area (Face> Torso > rarely the Buttocks), resulting in greasiness and polymorphic skin eruption.

3. Incidence:
Acne affect all skin types, the male and female ratio is virtually the same but tend to be more severe in males.
85% affect the age group 12 – 24 years
8% affect the age group 25 – 34 years
3% affect the age group 35 – 44 years

4. Etiology:
Genetic Aspect, (Acne runs in family) other example the case of severe acne that is associated with XXY syndrome.
Occupation (Environmental, Mechanical) e.g. exposure acnegenic mineral oil (Pomade acne) dioxin
Drugs Oral and topical Hydrocortison (Steroid acne) Lithium, Hydantoin, contraceptives
Endocrine Factors (Recalcitrant Acne, POD/s, MARSH Syndrome) .

5. Pathogenesis: ( three main steps recognized and hypothesized)
1. Follicular Hyperkeratosis (the cause not fully understood) theory suggest:
deficiency in Linoleic acid,
the effect off 5-a reductase enzyme on converting Androgen (Testosterone) hormone to the active acnegenic and potent (Dihydrotestosterone) DHT,
the direct effect of Interleukin-1 on follicular hyperkeratosis

6. Fig 1
Fig 2
Fig 3
Perifollicular Hyperkeratosis histology

7. Seborrhoea is a common feature between patients with acne.
2. Abnormal production of abnormal sebum increasing the ratio of wax easter to cholesterol and cholesterol easter and is believed to be the response of sebaceous glands to DHEA

8. 3. Colonization of the affected unit with bacteria Propionibacterium acne and yeast named Malassezia furfur
Fig 4
Fig 5
Malassezia furfur
Propionibacterium acne

9. P acne is potent activator of complement via classical pathway
Fig 6
Fig 7

10. Propionobacterium acne lipases act on sebaceous fatty acid (Triglycrides) to release irritant free fatty acid and low-molecular- weight peptide an extra cellular factor that penetrate the follicular wall and stimulate Polymorphs and Lymphocytes initiating inflammation
Fig 8

11. Hydrolytic enzymes released from the activated complement antibodies complex together with exoenzymes produced from P acne cause rupture of follicular wall
Fig 9

12. Once the wall is damaged Various agents (prostaglandin-like substance, amino acid, short chain fatty acid are) that are produced by the inflammatory cells and P acne extrude to the dermis causing more inflammation

13. Clinical features: (Acne and acne related Disorders)
Acne Vulgaris:
Papules: (Less than 0.5 cm)
Comedones (Open “Blackheads” or closed “Whitheads”)

14. Open Comedones (Blackheads)
Fig 10
Fig 11
Open Comedones

15. Closed Comedones (Whitehead)
Fig 12
Fig 13
Closed Comedones

16. Inflammatory papules
Fig 14
Fig 15
Inflammatory papules

17. Pustules :
Fig 16
Fig 17
Pustules

18. Nodule (more than 0.5 cm)
Fig 18
Fig 19
Nodule

19. Cystic acne: the cysts are usually large 1-4cm
Fig 20
Fig 21

20. 2. The nodules and cysts could be associated with sinuses as in Acne inversea
Acne inversea (Hidradinitis supprativa “a misleading name”) because it is considered by some to be disorder of apocrine gland (Sweat gland) but In my opinion Acne inversea affect primarily pilo Seb. Unit and affect secondarily the sweat gland, hence the correct name Acne inversea rather than Hidradinitis supprativa is preferred.

21. Fig 22

22. 3. Neonatal Acne and Infantile Acne
Neonatal acne: cause unknown but some believed is due to passing of Transplacental androgen other suggest the role of Mlalassezia furfur and sympodalis . affect 1 in 5 mainly inflammatory comedones on nose and cheeks affect new born between the 1st and 6th week of age

23. Fig 23

24. Infantile Acne: affect males more than females, usually between 3 and 6 months of age, and tend to be severer than the neonatal one and believed to be due to Endogenic androgen from the infant’s gonads.

25. Fig 24

26. 4. Recalcitrant Acne
Affect Women and associated with (Adrenal hyperplasia "11-B- or 21-B hydroxlase deficiencies) acne is usually nodulocystic

27. 5. Acne Fulminans
Affect youngsters 13 – 17 years of age, very severe with ulceration and puss discharge, associated symptoms include (fever malase myalgia arthritis and bone pain) laboratory investigation shows ESR
Can be induced by starting the patient on high dose of isotretinion (Roaccutane).

28. Fig 25

29. 6. Acne Conglobata
Very severe Acne, Nodulocystic form with abscess formation, affect Torso more than the face, usually associated with XYY Syndrome.

30. Fig 26
Fig 27

31. 7. Acne Agminata (Lupus Milliaris Disseminatus Faciei)
Some believe it is form of Rosacea (Granulomatous type), diagnosis is made at Histological base, Caseating Granulomata at the dermal level.

32. Fig 28

33. 8. Acne as part of other syndromes
MARSH Syndrome (Melsma, Acne, Rosacea, ,Seborrhoeic eczema, and Hirsutism)
Acne Conglobata
Favre Racouchot syndrome elderly with elastosis as part of Helioderma, sun exposure is a predisposing factor.
Polycystic ovarian syndrome
Atrophoderma vermiculatum as part of so called Ulerythema ophryogenes triat in Noonan Syndrome, de Lange Syndrome, and Rubinstein-Taybi Syndrome  Not considered acne

34. 9. Occupational I Environmental
Chloracne rare forms of acne affect patients exposed to Halogenated Hydrocarbons or who ingested Chlorinated Phenols (Dioxin)
Pomade acne or known as Oil Folliculitis
Acne Aestivalis or so called Mallorca Acne

35. Occupational II mechanical acne
Folicullitis Nuchae or so called Acne Keloidalis
Pseudofollicultis barbae
Acne excoriee as part of Psychodermatosis

36. TRAETMENT Note: All medications used for the treatment of acne act as:
Anti comedonal
Anti inflammatory
Anti microbial

37. Topical Keratolytic
Retinoid ( Retinoic acid 0.025, 0.05, 0.1%)
Adapelene (Diffrine 0.1%)
Salicylic acid
Benzoic acid
Azelaic Acid (10, 15, 20 %)

38. Topical Antibiotic
Topical clindamycin (Dalacin T)
Erythromycin
Mupirocin (Bactroban)
Sodium Fusidic acid (less significant in the treatment)

39. Systemic therapy
Antibiotic (Macrolides and Tetracyline)
Tetracycline
Doxycycline
Minocycline (Photo sensitivity and LE)
Erythromycines
Clarythromycines
Azithromycine

40. Systemic Retinoid
Isotretinoine caps (Roaccutane)
New promising and potentially safe medication SMT D002
Phase I clinical trial
Is believed to treat seborrhoea a symptom of Parkinson's disease and the primary cause of acne

41. Other form of therapy
Systemic steroid (Prednisolone) acne fulminans and intralesional steriods for forms of cystic acne.
Photodynamic therapy i.e. Laser therapy and phototherapy (Less significant)
Hormonal therapy (Antiandrogen)
Spironlacton (Potassium sparing agent) and Metformin as (Hypogylcemic agent) in treatment of POS have good results on acne

42. Fig 1, 2 www. scf-online. com/. /keratinization38_e
Fig 1, 2 keratinization of the duct of the hair follicle.
open (Blackheads) comedones, Medical Encyclopedia
Fig.3
Fig 4. Malassezia furfur Closed comedones Skin and allergy centre.
Fig 5
Fig 6 Mayo Foundation for Medical and research.
Fig 7
Fig 8 bacterial colonization
Fig 9 Breakage of follicular wall papule
Fig 10 open comedones
Fig 11
Fig 12 closed comedones
open and closed comedones schematic pictures
proriobionacterium acne in pilosabaceous unit
follicular hyperkeratosis in acne
Fig 13
Fig 14
Fig 15
Fig 16 pustule
Fig 17. Courtesy of Skin and allergy centre
Fig 18 nodule
Fig 19 nodule
Fig 20
Fig 21 Courtesy of Skin and allergy centre
Fig 22 Courtesy of Skin and allergy centre
Fig 23 at neonatal dermatology benign lesions Auckland district health board.
Fig 24 (infantile)
Fig 25
Fig 26 Courtesy of Skin and allergy centre
Fig 27 Acne conglobata
Fig 28 acne Agminata Granulomatous rosacea in infants. Report of three cases and discussion of the differential diagnosis João Borges da Costa, Sousa Coutinho V, L Soares de Almeida, M Marques Gomes PhDDermatology Online Journal 14 (2): 22

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